Arsenic retention in erythrocytes and excessive erythrophagocytosis is related to low selenium status by impaired redox homeostasis.
Arsenic retention in erythrocytes and excessive erythrophagocytosis is related to low selenium status by impaired redox homeostasis.
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砷在红细胞中的滞留和过度的红细胞吞噬作用与氧化还原稳态受损导致的低硒状态有关
DOI：
10.1016/j.redox.2022.102321
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发表时间：
2022-06
期刊：
影响因子：
11.4
通讯作者：
Huang, Zhi
中科院分区：
文献类型：
--
作者：
Cai, Zhihui;Zhang, Yutian;Zhang, Weijie;Ye, Jinmin;Ling, Qinjie;Xing, Zhi;Zhang, Sichun;Hoffmann, Peter R.;Liu, Youbin;Yang, Weidong;Huang, Zhi
饮用水砷污染是一个全球性的公共卫生问题。流行病学研究表明，硒（Se）缺乏与砷中毒的风险增加有关。然而，硒状态和作为保留在红细胞和这种关联的机制之间的关联还没有得到充分的研究。在本研究中，共招募了165名合格的受试者，发现As主要通过保留在红细胞中在血液中蓄积。红细胞中砷的存留与硒状态、抗氧化指标、硒甲基化能力呈负相关，而与砷的蛋白结合能力呈正相关。此外，从低硒状态受试者中分离的红细胞显示出细胞损伤沿着较低的CD 47蛋白水平，这可能会因过氧化氢治疗而加重。与人类研究一致，亚慢性砷暴露小鼠的红细胞表现出类似的细胞损伤，并被脾巨噬细胞吞噬，这些影响被膳食硒补充剂减轻。此外，过氧化氢处理诱导过度吞噬红细胞与脾巨噬细胞作为曝光，而共处理红细胞与还原剂，N-乙酰-L-半胱氨酸，减轻这种过度的红细胞吞噬。在过度吞噬红细胞后，在脾巨噬细胞中也检测到NFκB通路的过度活化。总之，本研究发现，低硒状态涉及受损的氧化还原稳态增加作为保留在红细胞，随后被吞噬的脾巨噬细胞，并导致脾巨噬细胞的炎症状态增加。这些研究结果提供了深入了解砷中毒的生理特征有关的硒状态和氧化还原稳态。低硒状态涉及受损的氧化还原状态诱导砷在红细胞中的保留。补充硒可减轻与红细胞吞噬作用相关的细胞损伤。吞噬含砷红细胞诱导脾巨噬细胞NFκB活化
Arsenic (As) contamination in drinking water is a global public health problem. Epidemiological studies have shown that selenium (Se) deficiency is associated with an increasing risk of arsenism. However, the association between Se status and As retention in erythrocytes and mechanisms underlying this association have not been fully investigated. In the present study, a total of 165 eligible subjects were recruited and As was found to accumulate in blood mainly by retention in erythrocytes. Retention of As in erythrocytes was negatively correlated with Se status, antioxidant parameters related to Se and As methylation capacity, but positively correlated with the protein-binding capacity of As. Additionally, erythrocytes isolated from subjects with low Se status exhibited cellular damage along with lower protein levels of CD47, which could be aggravated by hydrogen peroxide treatment. Consistent with the human study, the erythrocytes from mice with sub-chronic As exposure exhibited similar cellular damage and shown to be phagocytosed by splenic macrophages, and these effects were mitigated by dietary Se supplementation. Furthermore, hydrogen peroxide treatment induced excessive phagocytosis of erythrocytes with As exposure by splenic macrophages, while co-treating erythrocytes with the reducing agent, N-Acetyl-l-cysteine, mitigated this excessive erythrophagocytosis. Hyperactivation of the NFκB pathway was also detected in splenic macrophages after excessive erythrophagocytosis. In conclusion, this study found that low Se status involving impaired redox homeostasis increased As retention in erythrocytes, which were subsequently phagocytosed by splenic macrophages and led to an increased inflammatory status of splenic macrophages. These findings provide insight into physiological features of arsenism related to Se status and redox homeostasis. Low selenium status involving impaired redox status induces arsenic retention in erythrocytes. Selenium supplementation mitigates cellular damages related to erythrophagocytosis. Phagocytosis of arsenic-retained erythrocytes induced NFκB activation in splenic macrophages.
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